Parent Letter

This letter was an e-mail forwarded to us by Ralph Fucetola, JD

I am forwarding this interesting letter from Scott Blair, wst10999@rcvideo.com, to a number of alternative practitioners and others who might have some suggestions to him about his daughter’s vaccine induced diabetes. His letter contains significant observations and shows just how much progress informed parents can make when faced with Vaccine Injuries. The parents here have obviously sought alternative modalities and appear to have had some real success. If any of you have any further suggestions, please let the parents know.

To Scott: the government’s Vaccine Injury Compensation Plan (VICP) is at
http://www.hrsa.gov/osp/vicp/  I’ve posted a piece on the VICP on my
www.vitaminlawyer.com web site.

Also, have you been in touch with Dr. Carley, www.drcarley.com ? She has had some real success with nutrition and homeopathics in Vaccine Injury situations. You may want to explore the use of Thuja, the homeopathic which Broericke lists for vaccine reactions.

Ralph Fucetola, JD

Subject diabetes vaccines
Date Fri, 19 Jan 2001 07:59:38 -0500
From “Scott Blair” <wst10999@rcvideo.com>
To:  <ralph.fucetola@usa.net>

My Daughter at 8 years of age on August 18, 1999, developed type 1 diabetes. Since there was no family history on either side of my wife’s or my families side. And since everything we have read has said that it is always a genetic implication. So we decided since it was not hereditary, to look at any environmental factors that might have caused it. I read an article by Harris Coulter, Ph.D. President, Center for Empirical Medicine Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies April 16, 1997. Which indicated to me clear cut and dried evidence, that vaccines cause destruction of Beta Cells in the pancreas. I even found many other studies which said the same thing as well. Which I will attach at the end of this letter.

We immediately started looking for remedies at beta cell regeneration. We immediately put my daughter a product called Pancreas Tonic. A Natural Herbal remedy, that has been shown to regenerate Beta Cells in mice. Plus many other testimonies of people having success. My Daughter 1st C-Peptide test had shown she was .9 (.9-4.0 normal non-diabetic range). Her next C-Peptide test was 1.5. She went off of insulin during this time for 2 months. What the medical doctors call the honey moon phase. Then because of several colds, due to a suppressed immune system and putting a load on her immune system, her blood sugars started to elevate and we had to put her back on insulin again. And Her next C-Peptide test had shown she was 1.1. Being as everything we done was met with resistance from medical doctors, we finally found a doctor that would check her for live virus titers. She had shown she was very high with Mumps and Rubella and CMV. Also was high with Mercury Toxicity. Which is also found in vaccines. We were able to get rid of Mercury toxicity through a natural product called Chlorella, by a company from Japan called Sun. Who had a very good reputation. And her Mercury toxicity fell way below the normal ranges.

As far as the viruses. We have gone through a company called Chisholm’s laboratory that has a product used to get rid of live viruses. We used their products for 9 months now and hope very soon to be rid of these viruses. Also have been using products called olive leaf extract to help destroy these viruses as well. Plus using an ultra Beta product that they put out, to help reprogram the T-Cells to reprogram and build the immune system so that her immune system would quit attacking her beta cells along with the live viruses, in a process called Gad or Glutamic Acid Decarbyoxylase which causes an influx of Glutamic Acid and causes confusion in the immune system between determining what is foreign and what is not. Such as Viruses and Beta Cells. Since through Gad the viruses in combination with elevated Glutamic acid Mimic the Beta Cells. I don’t know the whole extent of this process but there are several studies that show that these all work in conjunction with these foreign viruses being introduced into the body causes this process to happen.

1. Do you have any suggestions as to how we could better reverse this process.

2. We would like to expose the Government and Pharmaceuticals companies to stop this genocide and sickness maintenance get rich quick scheme.

3. Are their any good lawyers that could help us pin those who are responsible for placing my daughter into a disease that has taken 15 % of her life from her. Placed into a life that looks forward to blindness, Amputation, Gangrene, Kidney disease, Cardiovascular disease just to name a small fraction.

4. And any other help that you might have or information that could help us reverse this dreadful disease would be greatly appreciated.

Incidentally my daughters latest C-Peptide test showed that she was “.8″. Meaning she has pretty much sustained her beta Cells. But I know the longer this process takes place the less likely she will ever reverse this diabetes. Since Vaccines are Politically correct. This process has cost us a lot of money being as the FDA will not allow anything that helps, to be funded by insurance.

Scott Blair
PO Box 73
Alma WV 26320
304-758-4388
sblair@rcvideo.com

Below is some of the Virus related info I have.

Childhood Vaccinations and Juvenile-Onset (Type-1) Diabetes

by Harris Coulter, Ph.D. President, Center for Empirical Medicine Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related
Agencies April 16, 1997

Diabetes, both juvenile-onset (Type I) and adult-onset (Type II), is a major health problem in the United States, and the number of diabetics is increasing every year.

In 1947, there were an estimated 600,000 cases of diabetes in the United States. (1)

Thirty years later, in 1976, Henry Bearn wrote:

It is perhaps not generally appreciated that in the United States diabetes, or at least the recognition of the disease, has increased about 300 percent over the last fifteen years. It is the second leading cause of blindness, and the third cause of death. In 1950 there were 1.2 million diabetics in the United States; the estimation now is that there are over 10 million, yet the population has increased by only 50 percent. (2)

Today the Metropolitan Life Insurance Co.’s quarterly Statistical Bulletin estimates that diabetics make up 5 percent of the US population, or 13 million persons. (3) Of these, 85-90 percent are adult onset, which is more or less controlled by diet and exercise; the other 10-15 percent require daily injections of insulin.

So, while the US population has approximately doubled since the 1940’s, the number of diabetics has risen more than 20 times. While the statistical data, like any medical statistics, are based to some degree on estimates, there has clearly been a huge increase in the number of diabetics in the United States.

Billions Spent to Help Diabetics – Furthermore, diabetics consumer about 15 percent of all health care costs, again according to Metropolitan Life. People not only die from diabetes (160,000 cases in 1994) but the disease leads to cardiovascular complications, stroke, gangrene of the extremities requiring amputation, kidney failure, and blindness.

With an estimated total health bill in the United States of about $1 trillion per year at the end of the 20th century, the annual bill for the care and treatment of diabetics will shortly amount to $100-$150 billion unless steps are taken to prevent this. If the Medicare and Medicaid expenditures for treatment of diabetics could be reduced by half, it would be a major savings.

African Americans At Risk – Of particular concern is the heightened prevalence of diabetes in the American black population. In 1991 the death rate from diabetes in American white males was 11.5/100,000 (resident population), for white females it was 9.6; for black males it was 24.6 and for black females it was 25.7. In other words, the death rate for blacks is 2-3 times as high as for whites (4).

This is an especially serious problem in the armed services. The expected incidence of Type-I (insulin-dependent) diabetes for persons aged 17-34 is 4/100,000 for whites and 90/100,000 for black sailors in the 17-34 age group. (5) The authors of this study admit ignorance about the reason why the diabetes incidence should be higher in black naval personnel.

Especially worrisome in this connection, is the ignorance of scientists about the reasons for the steep rise in diabetes. It may be due, in part, to earlier diagnosis or better treatment of the disease, thus preventing or postponing death and/or the development of stroke, kidney failure, and blindness. But this factor cannot account for the tremendous increase in cases since the 1940s.

Genetic and Environmental Factors – In any case, the very origin of diabetes is still a mystery. Since the late 19th century, diabetes has been known to be related to the pancreas and, in 1922, Canadians Frederick Banting and Charles H. Best, discovered that the missing factor was insulin – an internal secretion of the pancreas. But why does the pancreas stop, or fail to start, secreting insulin? Or, more specifically, why do the beta-cells of the pancreas cease to perform their functions?

The consensus on the causation of diabetes was expressed in 1976 in a paper by Alexander Bearn: Diabetes appears to be one of those diseases in which susceptibility may be inherited but where environmental factors may lead to the onset of disease and illness.” (6)

One environmental factor – viral infection – has been recognized; the other factor of significance for diabetes is the presence of an autoimmune process. (7) But the cause or causes of the epidemic of autoimmune disease in the United States, which commenced in the 1950’s, are themselves mysterious. (8)

Since the incidence and prevalence of diabetes continues to rise at a rather rapid rate in the United States and the other industrialized countries, every possible causal or environmental factor is worth examining. On such factor which has hardly been investigated at all is the relationship with childhood vaccinations. The purpose of my appearance here today is to draw the Committee’s attention to this connection.

No Investigation of the Vaccine Connection – As we will see, while there is much circumstantial and “anecdotal” evidence (meaning case histories) in favor of a diabetes/vaccination connection, this has never been officially investigated. The fact that the federal medical establishment – which would be the major source of funds for such an epidemiologic investigation – is itself highly committed to the childhood vaccination program, goes far to explain the absence of any official interest in this connection. This is a major  disadvantage of all research on damage from the childhood vaccination program.

In fact, several of the vaccines administered for the disease of childhood have been implicated in the causation of diabetes.

1. The Pertussis Vaccine
The vaccine for pertussis, or whooping cough, is part of the DPT shot (diphtheria, pertussis, tetanus) given to all children. The pertussis vaccine includes “pertussis toxin,” a toxin secreted by the microbe which causes whooping cough (the Bordetella pertussis). This toxin, which has been described as one of the most virulent poisons known to science, has several names and has a variety of effects on the body.

Pertussis Toxin Affects Pancreas – One of the names for pertussis toxin has traditionally been “islet-activating protein,” signifying that this substance acts specifically and directly on the “islets of Langerhans,” which are the insulin-secreting parts of the pancreas.(9)

At least since the 1970s, pertussis vaccine has been known in animal experiments to stimulate over-production of insulin by the pancreas followed by exhaustion and destruction of the “islets” with consequent under-production of insulin; in the first case the outcome is hypoglycemia, and in the latter it is diabetes. (10)

Physicians as early as 1949 called attention to low blood glucose in children who had severe reactions to the pertussis vaccine. (11) In 1970, Margaret Pittman wrote: “the infant whose blood sugar level is influenced by food intake may be especially vulnerable to vaccine-induced hypglycemia…the vaccine induces hypoglycemia in mice and rabbits.”

Gordon Stewart wrote in 1977: “more than any other vaccine in common use, pertussis vaccine is known pharmacologically to provoke…hypoglycemia due to increase production of insulin.” Two Dutch researchers, Hannik and Cohen, observed in 1978: “infants who show serious reactions following pertussis vaccination suffer from a failure to maintain glucose homeostasis.” And two German researchers, Hennessen and Quast, found in 1979 that 59 out of 149 children who manifested adverse reactions to the pertussis vaccine developed symptoms of hypoglycemia. (12)

The next logical step – deciding that the whooping cough vaccine could be responsible for the presently observed increase in the incidence of hypoglycemia and diabetes – has been inhibited by the federal government’s pro-vaccination policy, but enough researchers have spoken out in favor of a diabetes connection to suggest that this is a very real possibility deserving of further investigation.
II. The Measles-Mumps-Rubella Vaccine

The MMR (measles, mumps, rubella) vaccine, especially its mumps and rubella components, has been especially implicated in the causation of Type-I diabetes.

A. Rubella and the Rubella Vaccine

Of the three vaccines making up the MMR shot, the rubella component is the major suspect because rubella (German measles) itself, like mumps, is known to be a cause of diabetes and the action of the vaccine resembles that of the disease. If the disease can cause diabetes, so can the vaccine.

Let us first look at the disease.

Rubella Virus Causes Diabetes – In 1978 Margaret Menser wrote: “Since 1968 there has been increasing interest in the possibility that viral infection may play a part in the etiology of diabetes mellitus in man…[but] only one virus consistently produces diabetes in man – the congenitally acquired rubella virus.” (13)

“Congenital rubella syndrome” is the name given to the group of impairments and disabilities often seen in babies whose mothers become infected with rubella during pregnancy. These impairments include: heart disease, mental retardation, deafness, and blindness. E.J. Rayfield and colleagues wrote in 1986: “The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent [Type-I} diabetes mellitus.” (14)

In the 1960’s and 1970’s, researchers came to realize that the effect of the rubella virus does not end at the moment of birth, but that it remains in the organism of the baby and continues to exert its influence for many years thereafter. Especially to be noted is the fact that up to 20 percent of these individuals later come down with Type-I diabetes. This may take from 5 to 20 years to develop, indicating that the rubella virus remains active in the organism for all that time. (15)

This virus acts by forming “rubella-specific immune complexes” (an immune complex” is a mixture of the rubella virus and the antibody to it). P.K. Coyle and colleagues showed in 1982 that such immune complexes are found in individuals with congenital rubella and also in persons vaccinated against rubella. They were not found in persons who had never been infected with rubella nor in those who had had the disease naturally and recovered from it. These immune complexes can and do act on the pancreas. (16) In 1989, Numazaki and colleagues infected laboratory cultures of human pancreatic islet cells with rubella virus. They found that these infected cells produced much lower levels of insulin and concluded: these results suggest that rubella virus can infect human pancreatic islet cells and that such infection may lead to significant reductions in levels of secreted insulin.” (17)

Thus, rubella itself has been demonstrated to be a causal agent in Type-I diabetes.

How about the vaccine? Rubella Vaccine Virus Persists In Body – P.K. Coyle and colleagues demonstrated in 1982 that “rubella-specific immune complex formation is frequent after vaccination and could be demonstrated in two-thirds of an unselected group of vaccinates for as long as eight months after vaccination.” (18) In fact, the virus has been found to persist in the body of the vaccinated person for as long as seven years after vaccination. (19) This is not surprising, given that in congenital rubella syndrome the virus can persist for at least 20 years and, probably, for a lifetime. (20)

Thus, there is no reason to make a distinction between rubella virus entering the organism as part of the disease process and the same virus entering via a vaccination. It is known, for instance, that “vaccinees sometimes develop mild rubella, including rash, lymphadenopathy, fever, sore throat and headache.” (21) In adult women this occurs in about half the vaccinees. (22)

In both cases, immune complexes are formed and persist in the host organism for lengthy periods. Immune complexes from a vaccination can attack the pancreas just as easily as if they were from congenital rubella syndrome. The actual mechanism of such an attack on the pancreas is probably multifactorial. Aside from the possibility that the immune complexes attack the islet cells of the pancreas directly, there is also the likelihood that they generate an allergic (anaphylactic, hypersensitive) or autoimmune state with subsequent autoimmune destruction of the pancreas. Margaret Menser wrote: “Clinically it is not possible to show whether the pathogenesis of the diabetes initiated by the rubella virus is due solely to direct viral invasion of the beta-cells of the islets of Langerhans, or whether the virus induces an immunologic reaction in the islet cells, which then leads to the development of diabetes.” (23) E.J. Mayfield and colleagues wrote in the same connection:

“The mechanism of virus-induced diabetes is not known. Viruses associated with diabetes in animals may cause disease by (1) directly lysing [i.e., dissolving] the beta-cells; (2) triggering an autoimmune response; or (3) specifically impairing the secretory process of beta-cells through a persistent infection.” He concluded that option (2) was the most probable one: the generation of an autoimmune state in which the body, as it were, becomes allergic to itself or to a part of itself. (24)

The reasonableness of this explanation is enhanced by the observation that the rubella vaccine can cause an allergic reaction. (25) A Canadian survey in 1987 found “allergic reactions” in 30 children who reacted adversely to the MMR vaccine. (26) Indeed, the possibility of an anaphylactic reaction from the MMR vaccine is specifically recognized by the Vaccine Injury Table in Title 21 of the Public Health Service Act (this table was developed as a guideline for compensating victims of vaccination under the National Childhood Vaccine Injury Act of 1986, Public Law 99-660).

Diabetes after a rubella vaccination probably represents a combined effect: the virus attacks the islet cells of the pancreas in an organism which has already been weakened by an autoimmune reaction to the same virus.

B. Mumps and the Mumps Vaccine

Mumps Infection Can Cause Diabetes – There is copious evidence of a causal relationship between clinical mumps and subsequent development of diabetes. This evidence consists of: data linking mumps with pancreatitis; individual case reports of Type-I diabetes following clinical mumps infection; clusters of Type-I diabetes cases after mumps epidemics; and large epidemiological studies demonstrating parallel curves between outbreaks of mumps and new cases of Type-I diabetes (with a lag of 2-3 years). (27)

Furthermore, mumps virus can infect human pancreatic beta cells in vitro and destroy them. (28)

These and similar reports are noted and described in Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality (Washington, D.C: National Academy of Sciences, Institute of Medicine, 1993). This compendium was prepared by the Vaccine Safety Committee appointed as part of the overall effort of the federal government to evaluate vaccination risks and benefits as charged by the National Childhood Vaccine Injury Act of 1986 (100 Stat. 3780, 3781). The IOM Committee concluded:

“There is evidence suggesting that mumps virus infection can trigger the onset of Type-I diabetes in some individuals. Biologic plausibility data implicating the mumps virus in the pathogenesis of Type-I diabetes include: (1) the association between viral infections, including mumps, and Type-I diabetes in humans; (2) the detection of circulating autoantibodies against pancreaticantigens, particularly islet cells, during convalescence from mumps infection as well as early in the course of Type-I diabetes; and (3) in vitro studies demonstrating that the wild-type mumps virus can infect human pancreatic beta cells. (29)

The question to be answered is whether the mumps vaccine can have the same effect as the clinical infection with mumps.

Diabetes Reported Following Mumps Vaccination – There are many reports in the literature of Type-I diabetes emerging after mumps vaccination. In 1997, Sinaiotis and colleagues reported the onset of Type-I diabetes one month after receipt of mumps vaccine in a 6.5 year old boy. In 1991, Pawlowski and Gries described an 11-year old body who had mumps disease at age 16 months and then received measles-mumps vaccine 5 months prior to the emergence of Type-I diabetes; he had severe abdominal pain and fever one week after vaccination.

In 1984, Otten and colleagues reported three cases of Type-I diabetes with onset in one case 10 days and, in other cases, 3 weeks after mumps vaccination in children 3,2 and 16 years of age. In 1986, Helmke and colleagues reported seven children who developed Type-I diabetes in the second to fourth week following mumps or measles-mumps vaccination. In 1979, Quast and colleagues noted that in the first two years after mumps and measles-mumps vaccines were introduced into Germany, two cases of Type-I diabetes following immunization with measles-mumps and mumps vaccines respectively were reported to the manufacturer. (30) But, oddly enough, despite this finding and despite the series of case studies already noted, the Vaccine Safety Committee concluded that there was insufficient evidence either to accept or reject a causal relation between mumps vaccine and Type-I diabetes. This contradicted its own assertion in the Preface that: “In reaching conclusions favoring acceptance of a causal relation…the committee most commonly relied on case series and individual case reports.” (31)

C. Measles and Measles Vaccine

There is little convincing evidence of an association between measles as a clinical disease and diabetes; thus there is no reason to suspect the measles component of the MMR vaccine of any causal relationship to diabetes. (32)
III. Haemophilus Influenzae B and Hib Vaccine

A study of haemophilus influenzae B (Hib) vaccine in 114,000 Finnish children found that those who received 4 doses of the vaccine had a higher incidence of Type-I diabetes than those who received only one dose. (33)
IV. Hepatitis B and Hep-B Vaccine
According to J. Barthelow Classen, M.D., a hepatitis B vaccination program in New Zealand, which commenced in 1988, led to a 60 percent increase in Type-I diabetes in the recipients. In the under-20 age group, the incidence of Type-I diabetes prior to the vaccination campaign (i.e. from 1982-1991) was 18.2/100,000 person years.

Classen’s data have led the National Institute of Allergy and Infectious Diseases to request the Swedish health authorities to investigate the possible connection between the pertussis vaccine and Type-I diabetes. Results are expected to be available in several months.

In Classen’s view, the Hepatitis B vaccine and other vaccines can induce Type-I diabetes through the release of interferons, since interferons have already been implicated as causing autoimmunity, including Type-I diabetes. Classen also observes that the package inserts for the various hepatitis B vaccines on the market notes that they cause several autoimmune diseases, and the FDA itself has recognized that they can cause alopecia (baldness) of autoimmune origin. (34)
V. Conclusion
The vaccines discussed above are not an exhaustive list of those suspected of causing Type-I diabetes. Apparently in all cases, factors relating to autoimmunity are involved in the causal chain between vaccination and the emergence of Type-I diabetes. Any vaccine capable of giving rise to the autoimmune state is thus a candidate.

Little Research Exists on Vaccination and Autoimmunity – A 1996 article on vaccination and autoimmunity by researchers at Tel Aviv University in Israel throws additional light on this question. (35) The authors note that “in recent decades, although it has been suggested in case reports that some vaccines might trigger autoimmune disorders, the subject has received comparatively little attention in clinical and laboratory studies.”

Such vaccines as influenza, hepatitis A, hepatitis B, rabies, MMR, tetanus and oral polio have all been linked with autoimmune diseases such as reactive arthritis, thrombocytopenia purpura and lupus. Also, the authors note, “it seems that vaccines have a predilection to affect the nervous system: neuritis, demyelination, myasthenia gravis, and Guillain-Barre syndrome have been described.” Furthermore, the incidence of vaccine-induced autoimmunity is twice as high as high in females as in males. The authors conclude: “The subject of the vaccine autoimmunity relationship is still obscure; reports have been rare, not laboratory experimentation on this topic has been undertaken, and there are few animal models. For the time being no conclusions can be drawn.”

Since this is still virgin territory, we may expect far more data in support of the vaccine-autoimmunity connection as work progresses and, specifically, on the connection with Type-I diabetes.

Military and African American Populations Need Study – Further evidence of a possible vaccination link is found in the data on diabetes in US Navy enlisted personnel mentioned above. These are individuals in whom Type-I diabetes has appeared after the age of enlistment (since diabetes is a bar to enlistment). Frequent vaccinations seems to be a fact of life in the US armed forces. In the absence of any suggestion as to other possible causative factors which could transform a healthy sailor into a diabetic, the vaccinations which these men and women receive at regular intervals during their naval service must be considered as prime suspects. (36)

The greater incidence of diabetes in the US African American population can readily be explained in terms of enhanced susceptibility to vaccine damage. The genetic background of this population may differ in significant respects from that of white populations sufficiently to account for a greater likelihood of vaccine damage.

Public Health Agencies Ignore Diabetes-Vaccine Connection – A striking feature of this whole diabetes/vaccination picture is the division or bifurcation of medical opinion. While researchers are well aware of the significance of vaccinations as etiological agents in the production of diabetes, the Public Health Service and related agencies promoting vaccination programs deny or ignore this relationship or are simply unaware of it. At any rate, the public is not yet being informed of this additional and very real risk from the vaccines which they are compelled to administer to their children.

The seriousness of Type-I diabetes is perhaps not appreciated by the public at large. While not quite a death sentence, it is close to it. Panzram wrote in 1984: “Type-I diabetes, particularly at a young age, must be considered as a rather serious disease, with a 5 to 10-fold higher excess in mortality in comparison with the general population.” (37)

Diabetes is the seventh leading cause of death in the United States. Type-I, especially, means a shortened life with many disagreeable features such as stroke, kidney failure, cardiovascular complications, blindness and the need to amputate gangrenous limbs. The bill for treating these conditions is, as already noted earlier, in the neighborhood of $100-$150 billion every year.
VI. Suggestions for Action
As noted throughout this paper, the Public Health Service and other federal health agencies promote vaccination programs and do not readily criticize them. Even the scanty information we have today about vaccine damage would not have been available if the Congress had not adopted the National Childhood Vaccine Injury Act of 1986 (over a presidential veto), compelling these agencies to investigate areas they would have preferred to ignore.

The following action items are suggested as ways to prevail on these agencies to pursue further research on these matters and thus increase our knowledge of the vaccination-diabetes connection.

Study Military Personnel – An effort should be made to contact former armed services personnel who contracted Type-I diabetes while on active service. Since diabetes is a bar to military service, one can be relatively certain that these individuals were diabetes-free at the time of enlistment. It would be interesting to ascertain the chronological relationship between one or another of the many vaccinations received by servicemen and women and the date of onset of the first symptoms of diabetes (the testimony of one who did contract diabetes in this way is given in the Appendix).

Study Modification of Vaccination Schedules – Alternative scheduling of childhood vaccinations as a way of minimizing the incidence of Type-I diabetes should be studied.

Conduct Cost-Benefit Analyses – Cost-benefit analyses of various childhood vaccines should be prepared based on the assumption that they contribute to the incidence of Type-I diabetes.

Alert Doctors – Physicians should be alerted to Type-I diabetes as a possible consequence of rubella, pertussis and other childhood vaccinations; if that were done, the reporting of Type-I diabetes would be intensified.

Add Type-I Diabetes to Vaccine Injury Compensation Table – Consideration should be given to including Type-I diabetes in the Vaccine Injury Table of the national vaccine injury compensation program created under PL99-660.

NOTES

1. Henry A. Christian, The Principles and Practice of Medicine. Sixteenth Edition. New York: D. Appleton-Century, 1947, 582.

2. Alexander G. Bearn, “Structural Determinants of Disease and Their Contribution to Clinical and Scientific Progress.” SIBA Foundation Symposiums 44 (1976), 25-40, at 28.

3. Washington Post. Health. April 1, 1997.

4. USDHHS, Health United States 1993. Washington, D.C: GPO, 1994-93.

5. Edward D. Gorham, Frank G. Garland, Elizabeth Barrett-Connor, Cedric F. Garland, Deborah L.
Wingard and William M. Pugh, “Incidence of Insulin-dependent Diabetes Mellitus in Young Adults:
Experience of 1,587,630 US Navy Enlisted Personnel.” A.J. Epidemiology 138:11 (1993), 984-987.

6. Alexander Bearn, op cit, 36-37.

7. Daniel P. Stites, John D. Stobo, H. Hugh Fudenberg and J. Vivian Wells, Basic and Clinical Immunology. Fifth Edition. Los Altos, California: Lange, 1984, 152ff.

8. Ibid., 153.

9. H.L. Coulter and Barbara Loe Fisher, DPT: A Shot in the Dark, Garden City Park, N.Y.: Avery Publishers, 1991, 49-50.

10. Ronald D. Sekura, Joel Moss and Martha Vaughan, Pertussis Toxin. New York and London:

Academic Press, 1985, 19-43; J.J. Munoz and R.K. Bergman, Bordetella Pertussis. New York and Basel: Marcel Dekker, 1977, 160ff.; B.L. Furman, A.C. Wardlaw and L.Q. Stevenson, “Bordetella Pertussis-Induced Hyperinsulinemia Without Marked Hypoglycemia: A Paradox Explained.” British Journal of Experimental Pathology 62 (1981), 504-511.

11. Cited in C.S.F. Easmon and J. Jeljaszewicz, Medical Microbiology, Volume 2. Immunization Against Bacterial Diseases. London and New York: Academic Press, 1983, 246.

12. Cited in H.L Coulter and Barbara Loe Fisher, op. cit., 49-50.

13. Margaret Menser et al., “Rubella Infection and Diabetes Mellitus.” Lancet (January 14, 1978), 57-60, at 57.

14. E.J. Rayfield et al, “Rubella Virus-Induced Diabetes in the Hamster.” Diabetes 35 (December, 1986), 1278-1281, at 1278.

15. Ibid., 1280. Daniel H. Gold and T.A. Weingeist, The Eye in Systemic Disease. Philadelphia:

Lippincott, 1990, 270.

16. P.K. Coyle et al., “Rubella-Specific Immune Complexes After Congenital Infection and Vaccination.”
Infection and Immunity 36:2 (May, 1982), 498-503, at 501.

17. Kei Numazaki et al. “Infection of Cultured Human Fetal Pancreatic Islet Cells by Rubella Virus.” A.J. Clinical Pathology 91 (1989), 446-451.

18. P.K. Coyle et al, op. cit., 501.

19. Ibid, 502. Wolfgang Ehrengut, “Central Nervous System Sequelae of Immunization Against Measles, Mumps, Rubella and Poliomyelitis.” Acta Paediatrica Japonica 32 (1990), 8-11, at 10; Aubrey J. Tingle et al., “Postpartum Rubella Immunization: Association with Development of Prolonged Arthritis, Neurological Sequelae, and Chronic Rubella Viremia.” J. Infectious Diseases 152:3 (September, 1985), 606-612, at 607.

20. E.J. Rayfield et al., op. cit., 1281.

21. Stanley A. Plotkin and Edward Mortimer, Jr., Vaccines. Philadelphia: W.B. Saunders Co., 1988, 248.

22. M. Poyner et al., “The Reactogenicity of Rubella Vaccine in a Population of United Kingdom Schoolgirls.” B.J. Clinical Practice 40:11 (November, 1986), 468-471, at 470.

23. Margaret Menser et al., op. cit, 59.

24. E.J. Rayfield et al., op. cit., 1278, 1280.

25. T.M. Pollock and Jean Morris, “A 7-Year Survey of Disorders Attributed to Vaccination in North West Thames Region.” Lancet (April 2, 1983), 753-757, at 754.

26. Sasson Lavi et al., “Administration of Measles, Mumps and Rubella Vaccine (Live) to Egg-Allergic Children.” Journal of the AMA 263:2 (January 12, 1990), 269-271.

27. Kathleen R. Stratton et al, editors, Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality, Washington, D.C.: National Academy Press, 1993, 153-154.

28. Ibid, 156.

29. Ibid, 158-159.

30. Ibid, 154.

31. Ibid, vi.

32. Kathleen R. Stratton, et al., opc. cit., 154, 158.

34. J. Barthelow Classen, “Childhood Immunisation and Diabetes Mellitus.” New Zealand M.J., 109 (May 24, 1996), 195.

35. Arnon Dov Cohen and Yehuda Shoenfeld, “Vaccine-Induced Autoimmunity.” J. Autoimmunity 9 (1996), 699-703.

36. Edward D. Gotham et al, op. cit.

37. G. Panzram, “Epidemiologic Data on Excess Mortality and Life Expectancy in Insulin-Dependent Diabetes Mellitus – Critical Review.” Exp. Clin. Endocrinol. 83: 1(1984), 93-100, at 93.

And also

In the May 24, 1996 New Zealand Medical Journal, Dr. Classen reported that there was a 60 percent increase in Type I diabetes (juvenile diabetes) following a massive campaign in New Zealand from 1988 to 1991 to vaccinate babies six weeks of age or older with hepatitis B vaccine. His analysis of a group of 100,000 New Zealand children prospectively followed since 1982 showed that the incidence of diabetes before the hepatitis B vaccination program began in 1988 was 11.2 cases per 100,000 children per year while the incidence of diabetes following the hepatitis B vaccination campaign was 18.2 cases per 100,000 children per year.

More Vaccines Equal More Diabetes – In the October 22, 1997 Infectious Diseases in Clinical Practice, Classen presented more data further substantiating his findings of a vaccine-diabetes connection. He reported that the incidence of diabetes in Finland was stable in children under 4 years of age until the government made several changes in its childhood vaccination schedule. In 1974, 130,000 children aged 3 months to 4 years were enrolled in a vaccine experimental trial and injected with Hib vaccine or meningococcal vaccine. Then, in 1976, the pertussis vaccine used in Finland was made stronger by adding a second strain of bacteria. During the years 1977 to 1979, there was a 64 percent increase in the incidence of Type 1 diabetes in Finland compared to the years 1970 to 1976.

In 1982, another vaccine was added to the childhood vaccination schedule in Finland. Children aged 14 months to six years were given the live MMR (measles-mumps-rubella) vaccine. This was followed by the injection of 114,000 Finnish children aged 3 months and older with another experimental Hib vaccine. In 1988, Finland recommended that all babies be injected with the Hib vaccine.

The introduction of these new vaccines in Finland were followed by a 62 percent rise in the incidence of diabetes in the 0 to 4 year old age group and a 19 percent rise of diabetes in the 5 to 9 year old age group between the years 1980 and 1982 and 1987 and 1989. Classen concluded:”The net effect was the addition of three new vaccines to the 0-4 year old age group and a 147 percent increase in the incidence of IDDM [insulin dependent diabetes mellitus] , the addition of one new vaccine to the 5-9 year olds and a rise in the incidence of diabetes of 40 percent, and no new vaccines added to the 10 to 14 year olds and a rise in the incidence of IDDM by only 8 percent between the intervals 1970-1976 and 1990-1992. The rise in IDDM in the different age groups correlated with the number of vaccines given.”

“The results indicate that previous vaccine trials are flawed because they are not designed to detect associations between vaccination and autoimmune diseases, such as IDDM. Prospective clinical trials are needed to further evaluate the effect of vaccines on IDDM.”

Thank you Scott Blair